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What shunts close at birth
foramen ovale, ductus venosusm ductus arteriosis
murmurs
heart sounds that reflect the flow of blood within the heart
may occur during systole, diastole or both
3 classifications of heart murmurs
innocent -> noise from normal blood flow
functional -> increased cardiac output
organic -> structural change in the heart
Heart sounds
S1 -> closure of tricuspid and mitral valves
S2 -> closure of aortic and pulmonic valves
Congenital heart disease (CHD) - incidence/causes
5-8 in 1,000 births
higher than normal with
- maternal rubella (measles) or viral illness
- poor prental nutrition
- maternal alcoholism
- maternal age over 40
- maternal diabetes
Acyanotic heart defect
blood is shunted from the left side to right side of heart due to structural defect in the interventricular septum
often retain normal levels of oxyhemoglobin sats in circulation (normal spo2 levels makes hard to tell because child will present as normal)
- VSD, ASD, PSD, coarctation
What is an atrial septal defect (ASD)?
A condition where the wall between the right and left atria does not close properly, leaving a hole between the two atria.
What is the incidence rate of atrial septal defect (ASD)?
4 in 100,000.
How does atrial septal defect (ASD) typically present when no other congenital defect coexists?
ASD may present asymptomatically, possibly with a slight murmur.
Does atrial septal defect (ASD) usually require intervention?
It often closes on its own most times.
Treatment: ASD
patients with cardiac defects are at higher risk for infection
often closes on its own
surgical repair depends on size
catheter-based repair or open-heart surgery to repair ASD
Cardiac Catheterization
Cannulation of a vein, usually in groin or neck area to pass catheter into heart or major vessels of heart
advanced with the use of x-ray fluroscopy
keep extremetits striaght for 4-6 hours with no movement; position flat on back
foley catheter may be used
check pulses above and below site (normal for pulse BELOW site to be weaker post op due to disruption of blood flow)
Auscultate for abnormal HR or rhythm and compare to pre op
monitor for bleeding with pressure dressing for 24 hours then dry occlusive dressing (bandaid, gauze, tape)
monitor for temp or color changes (check cap refill - if pale/cold blood flow not adequate)
no tub baths
observe S&S of infection
fever is common but should not last longer than 24 hours or be above 100 degrees
Risks of cardiac cath
acute hemorrhage from entry site
nausea and vomiting
loss of pulse in catheterized extremity
cardiac arrhythmia
Ventricular septal defect
abnormal opening in the wall that separates the R and L ventricles
0.4% born with
degree depends of size of defect with up to 75% of small defects closing spontaneously
Most babies are asymptomatic and hole repairs on their own
Symptoms of VSD
asymptomatic with murmur
SOB
feeding difficulties (heart in overdrive burns more calories)
murmur
FTT -> not gaining weight
recurrent respiratory infections
treatment of VSD
cardiac cath or surgical repair
Patent Ductus Arteriosus
ductus arteriosis closes shortly after birth if it does not close then it is patent ductus arteriosus
An abnormal opening between the aorta and pulmonary artery
Clinical manifestations: PDA
all or nothing (asymptomatic or CHF) (difficutly breathing and arrythmias
MACHINE LIKE MURMUR
tachycardia
bounding pulses
fatigue
FTT/poor eating
**widened pulse pressure**
low diastolic
Pulse Pressure
120/80 = 40 PP, if higher can indicate PDA
Tx: PDA
Indomethacin (Indocin)/ibuprofen
surgery to ligate artery via L thorcatomy
video assisted thorascopic surgery
Preventing bacterial endocarditis
PDA/ASD/VSD -> risk factor for it
caused by irritation of smooth muscle tissue -> created favorable medium for bacterial growth
antibiotics before oral, dental, or respiratory procedures
Co-arctation of the aorta
narrowing of the aorta between upper body and lower extremities
increased BP to head
decrease BP in the lower extremities
Clinical manifestations: co-arctation
majority start asymptomatic -> grow and develop normally
- 20-30% develop CHF by 3 mo -> no symptoms so goes undiagnosed
*higher BP in arms than legs
characteristic murmur heard at R midline or lower sternal border
**weak femoral pulses, cool legs
Leg pain can be confused for growing pains, but it is actually from a lack of blood
headache
Tx: co-arctation
ballon dilation for intital relief through umbilical artery in infants
surgical resection with end-end anastomosis -> cut and reattach
Pulmonic stenosis
Narrowing of the entrance to the pulmonary artery and resistance to blood flow cause right ventricular hypertrophy and decreased pulmonary blood flow
Symptoms: pulmonic stenosis
**SOB
cyanosis
murmurs
tx: pulmonic senosis
nonsurgical: balloon angioplasty in cath lab to dilate valve
surgical: valvotomy
Aortic stenosis
narrowing of aortic valve
causes increased resistance in the left ventricle, decreased cardiac output, and left ventricular hypertrophy
Symptoms: aortic stenosis
**faint pulses
**hypotension
poor feeding
tachycardia
murmur
exercise intolerance
chest pain
dizziness with standing
Treatment: aortic stenosis
same as pulmonic stenosis
cyanotic heart defect
deoxygenated blood bypasses the lungs and enters systemic circulation
right-to-left shunting, bidirectional shunting, malposition of the great arteries
Tetralogy of Fallot
birth defect of the heart consisting of 4 abnormalities (results in insufficiently oxygenated blood pumping to the body)
- pulmonic stenosis
- right ventricular hypertrophy
- overriding aorta
- VSD
Symptoms: TET
may not show cyanosis at birth but develop episdoes later
*blue spells or tet spells
characteristic murmur
at risk for seizures, LOC, sudden death
TET spell intervention
Place the child on its side, pull the knees up to the chest, and calm the baby
TET: interventions/parent education
feed child slowly
give smaller more frequent meals
decrease anxiety by being calm
knee-chest position
miinimize crying by anticipating child needs
Prepare the family for the possibility of multiple surgeries
transposition of the great vessels
when the aorta and pulmonary artery are transposed
cyanotic defect because it results in insufficiently oxygenated blood pumped to the body
*pulmonary artery exits left ventricle
*aorta exits right ventricle
most common cyanotic identified in first week of life
no communication between pulmonary and systemic circulation
usually associated with other defects such as ASC]D/PDA/VSD to permit blood to mix
even though oxygenated blood is mixed with non it is not enough to sustain life
**extremely blue at birth
Treatment: transposition of the great vessels
*GOAL: increase blood oxygenation
IV prostaglandins: keep ductus arteriosus open (allows blood flow to body)
Surgery: arterial switch
- done in first few weeks
- switching and re-establishing coronary arteries to establish normal circulation
- creates new aorta
*neurological and developmental complication risk is high after surgery
Hypoplastic left heart syndrome
underdevelopment of the left side of heart resulting in small aorta and left ventricle
*will have PDA and ASD in order to have blood flow through heart
Descending aorta receives blood from the ductus arteriosus
Clinical manifestations: Hypoplastic left heart
before PDA closes
- mild cyanosis
after PDA closes
- progressive deterioration with cyanosis and decreased cardiac output leading to cardiovascular collapse
skin is cold and clammy
cyanosis
abnormality in breathing
poor feeding
Treatment: hypoplastic left heart
maintenance of PDA with prostaglanding E (vasodilate it until surgery)
surgery (can be fixed but in severe cases need transplant)
heart transplant
post-op complications: hypoplastic left heart
imbalance of systemic and pulmonary blood flow
bleeding
low cardiac output
persistent heart failure
post-op concerns: hypoplastic left heart
cardiac tamponade-> compression of heart
hypothermia -> warm slowly post-op
chest tube drainage (over 3mL/kg/hr or 10-15mL/kg any hour is exessive and a problem)
SVT - superventricular tachycardia
occurs in atria
HR >220 BPM
stimulate vagal response with cold to reset heart
apply ice to forehead
adenosine IV push
Congestive heart failure
heart pumps well but very insufficient due to a structrual problem
can be result of a weak heart muscle that does not pump a normal amount of blood to the body
"rubberband theory" - the more you use it, the less it will work
CHF - impaired myocardial function
edema, poor feeding, sweaty with feeding, minimal activity, FTT, SOB, cyanosis
pulmonary congestion
sudden wt gain, tachypnea, tachycardia, increased respiratory effort
systemic venous congestion
bulging neck veins (jugular venous distention)
CHF - manifestations
poor growth
heart failure
sweaty with feedings
lungs fill with fluid
chest and belly muscles to help breathe
weight gain from edema
hepatomegaly
CHF - DX
chest x-ray
exercise test
echocardiogram
cardiac cath
MRI to see heart function
Treatment - CHF
surgery or heart transplant
Furosemide -> eliminates extra fluid in lungs
- first line med for edema
-> encourage eating potassium because diuretics pull it from body
ACE inhibitors (captopril) decrease BP or beta blockers (propanolol)
-> theoretically lowering BP will decrease workload of heart and relax it
Digoxin: improve contractility of heart and help pump blood more efficiently by slowing HR
high potassium foods
avacado, banana, potatoes, spinach, beans, citrus juices, fish
Digoxin
*can be easily over- or under-medicated
be aware of baseline parameters: pulse, BP, HR
Administer 1 hour before or 2 hours after meals
-> if child vomits DO NOT repeat dose
take apical pulse for full minute
-> changes in HR especially bradycardia is first sign of digoxin toxicity
monitor for S&S of digoxin toxic effects:
-> anorexia, nausea/vomiting, diarrhea, and visual disturbances
frequent blood draws to check dosin levels
*DUAL SIGN OFF MED*
caregiver education - digoxin
give at same time everyday -> do not double if dose is missed
nofity PCP before giving OTC meds
*DO NOT breastfeed if child is taking (can be absorbed through breast)
digoxin toxicity = vomiting
too low a dose = tired, lethargic, edema
ABCD of CHF
A- ACE inhibitors
B- Beta blockers
C - concentrated calories (fortified formula)
D - Digoxin/diuretics
Shock
inability of body to maintain adequate blood flow and oxygen supply to the tissues needed for metabolism
- 3 types
hypovolemic shock
profound dehydration or loss of blood with a decrease in hemoglobin; X-ray would show a normal heart
cardiogenic shock
Damage to the heart muscle resulting in pump failure
septic or distributive shock
shifting of fluids from the intravascular space to the extracellular space; caused by blood vessel dilation, often a result of sepsis (some sort of infection)
Shock treatment
fluids
blood and blood products
antibiotics
medications to increase BP and the delivery of oxygen to tissues
shock assessment
confusion or lack of alertness
LOC
sudden rapid heartbeat
sweating
pale skin
weak pulse
rapid breathing
decreased or no urine output
cold hands and feet